Evidence map›Paper›PMID 30389701›Full record

ArticleCancer research2019

Activation of PP2A and Inhibition of mTOR Synergistically Reduce MYC Signaling and Decrease Tumor Growth in Pancreatic Ductal Adenocarcinoma.

Brittany L Allen-Petersen, Tyler Risom, Zipei Feng, Zhiping Wang, Zina P Jenny, Mary C Thoma, Katherine R Pelz, Jennifer P Morton, Owen J Sansom, Charles D Lopez and 5 more

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.4field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

57 citing papers in PubMed, 90 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Targeting PP2A in cancer: an underrated option.Journal of experimental & clinical cancer research : CR · 2025
    Review
  9. Proteomics in pancreatic cancer.Biomarker research · 2025
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. The next decade of SET: from an oncoprotein to beyond.Journal of molecular cell biology · 2024
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 2 countries.

Brittany L Allen-PetersenDepartment of Molecular and Medical Genetics, Oregon Health and Science University, Portland, Oregon.ORCID 0000-0002-7436-9412
Tyler RisomDepartment of Molecular and Medical Genetics, Oregon Health and Science University, Portland, Oregon.
Zipei FengDepartment of Cell, Developmental & Cancer Biology, Oregon Health and Science University, Portland, Oregon.
Zhiping WangDepartment of Molecular and Medical Genetics, Oregon Health and Science University, Portland, Oregon.
Zina P JennyDepartment of Molecular and Medical Genetics, Oregon Health and Science University, Portland, Oregon.
Mary C ThomaDepartment of Molecular and Medical Genetics, Oregon Health and Science University, Portland, Oregon.
Katherine R PelzDepartment of Molecular and Medical Genetics, Oregon Health and Science University, Portland, Oregon.
Jennifer P MortonCRUK Beatson Institute, Glasgow, Scotland, United Kingdom.
Owen J SansomCRUK Beatson Institute, Glasgow, Scotland, United Kingdom.
Charles D LopezDepartment of Hematology and Oncology, Oregon Health and Science University, Portland, Oregon.
Brett SheppardDepartment of Surgery, Oregon Health and Science University, Portland, Oregon.
Dale J ChristensenOncotide Pharmaceuticals, Inc., Research Triangle Park, North Carolina.
Michael OhlmeyerIcahn School of Medicine at Mount Sinai, New York, New York.
Goutham NarlaSchool of Medicine, Case Western Reserve University, Cleveland, Ohio.
Rosalie C SearsDepartment of Molecular and Medical Genetics, Oregon Health and Science University, Portland, Oregon. searsr@ohsu.edu.
Oregon Health & Science University · USCancer Research UK Scotland Institute · GBCase Western Reserve University · USIcahn School of Medicine at Mount Sinai · USResearch Triangle Park Foundation · US

Funding

Understanding the origins of rapid recurrence of pancreatic cancer after resectionP30CA069533 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI Luiz Eduardo Bertassoni · 1997 to 2026
$60.5M
Understanding the Impact of Microscale and Nanoscale Heterogeneity and ResistanceU54CA209988 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI DEMIR, EMEK, HEISER, LAURA MADELINE · 2017 to 2021
$10.3M
Hydroxylation regulation of c-MycR01CA186241 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI Mu-Shui Dai, ROSALIE C SEARS · 2015 to 2026
$4.2M
Cellular Mechanisms Controlling Myc Protein StabilityR01CA100855 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI SEARS, ROSALIE C · 2003 to 2014
$3.6M
The Role of post-translational activation of Myc in pancreatic cancerR01CA196228 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI SEARS, ROSALIE C · 2015 to 2019
$2.0M
c-Myc Phosphorylation Sites Regulate Its Apoptotic and Tumorigenic PotentialR01CA129040 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI SEARS, ROSALIE C · 2008 to 2012
$1.6M
MYC is a critical downstream effector in KRAS-driven pancreatic cancerF32CA192769 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI ALLEN-PETERSEN, BRITTANY · 2015 to 2017
$176k
Cancer Research UK 21139Cancer Research UK 29996NCI NIH HHS F32 CA192769NCI NIH HHS P30 CA069533NCI NIH HHS R01 CA100855NCI NIH HHS R01 CA129040NCI NIH HHS R01 CA186241NCI NIH HHS R01 CA196228NCI NIH HHS U54 CA209988
6 · The paper itself

Abstract

In cancer, kinases are often activated and phosphatases suppressed, leading to aberrant activation of signaling pathways driving cellular proliferation, survival, and therapeutic resistance. Although pancreatic ductal adenocarcinoma (PDA) has historically been refractory to kinase inhibition, therapeutic activation of phosphatases is emerging as a promising strategy to restore balance to these hyperactive signaling cascades. In this study, we hypothesized that phosphatase activation combined with kinase inhibition could deplete oncogenic survival signals to reduce tumor growth. We screened PDA cell lines for kinase inhibitors that could synergize with activation of protein phosphatase 2A (PP2A), a tumor suppressor phosphatase, and determined that activation of PP2A and inhibition of mTOR synergistically increase apoptosis and reduce oncogenic phenotypes

Indexed as

Drug SynergismAdenineAnimalsApoptosisBenzoxazolesCarcinoma, Pancreatic DuctalEnzyme ActivationHumansMicePancreatic NeoplasmsProtein Phosphatase 2Proto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycPyrimidinesSmall Molecule LibrariesTOR Serine-Threonine KinasesAdenineBenzoxazolesMTOR protein, humanProtein Phosphatase 2Proto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycPyrimidinessapanisertibSmall Molecule LibrariesTOR Serine-Threonine Kinases

Identifiers

PMID30389701
PMCPMC6318036
OpenAlexW2899353968

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.